The human heart is a muscular organ that functions as two parallel two-stage pumps. Blood is delivered to the left and right ventricles by left and right auricles when the ventricular muscles are relaxed. Then, the ventricular muscles contract and forcefully pump the blood through arteries. If the ventricular muscles are not adequately relaxed or are in a state of rigor during diastole, that is when blood flows into the ventricles, the ventricular filling volume is reduced and the amount of blood which can be pumped from the heart with each beat is reduced. Further, any rigidity of the ventricular muscle, whether due to contracture of the muscle or a passive inelasticity, also reduces the amount of blood which can be pumped into the ventricle during the diastolic state. Once the ventricle is filled to a diastolic volume, as limited by any diastolic rigor, contracture, passive elasticity or diastolic compliance, the contraction of the ventricular muscle pumps that volume of blood into the arteries. The strength of that pumping action is another indication of the condition of the heart.
During heart surgery the heart is bypassed by a mechanical blood pump, and the heart is arrested to enable the surgeon to operate. The ventricular chamber is evacuated and, conventionally, the supply of blood to the coronary arteries to oxygenate the heart muscles is cut off, resulting in global ischemia.
Prolonged myocardial arrest, particularly in combination with ischemia or hypoxia, results in myocardial rigor or contracture. During the ischemic arrest of cardiac surgery this process is recognized in its most extreme form as the "stone heart" syndrome. Mild degrees of contracture which do not cause the fullblown stone heart syndrome can significantly decrease diastolic ventricular compliance, impede diastolic ventricular filling and reduce cardiac output. Two recent clinical reports indicate that such a decrease in left ventricular diastolic compliance commonly occurs in patients undergoing open heart surgery, especially when the period of ischemic arrest lasts longer than 40 minutes. Spotnitz et al., "Effects of open heart surgery on end-diastolic pressure--diameter relations of the human left ventricle," Circulation 59: 662-671, 1979, and Chitwood et al., "Effects of global ischemic arrest on ventricular compliance in man as determined by pulse transit sonomicrometry," Am J Cardiol 43: 378, 1979. Ischemic contracture appears to result from the formation of rigor bonds between actin and myosin. These bonds form when the intracellular adenosine triphosphate concentration falls below a critical level, and the contracture process itself further accelerates the hydrolysis of adenosine triphosphate.
An object of the invention is to provide means for protecting an arrested heart against the deleterious effects of a sustained arrest and, particularly, of an ischemic arrest.